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ENVIRONMENTAL CARCINOGENESIS IN THE MUMMICHOG, FUNDULUS HETEROCLITUS: FIELD AND LABORATORY INVESTIGATIONS
Citation:
Vogelbein, W. K., D. E. Zwerner, M. A. Unger, P. A. Van Veld, AND J W. Fournie. ENVIRONMENTAL CARCINOGENESIS IN THE MUMMICHOG, FUNDULUS HETEROCLITUS: FIELD AND LABORATORY INVESTIGATIONS. Presented at Aquaria Fish Models of Human Disease, Southwest Texas State University, San Marcos, TX, 21-24 September 2000.
Description:
The mummichog, Fundulus heteroclitus, is a small estuarine teleost inhabiting coastal embayments along much of the eastern seaboard of the US. We have been investigating an association between chemical contaminant exposure and adverse health impacts in this small cyprinodontid fish because it is an excellent environmental sentinel species and laboratory model of chemical carcinogenesis. Much of our research has focused and continues to focus on a localized population inhabiting a creosote-contaminated environment in the Elizabeth River, VA. Our field investigations at this site and elsewhere in the Chesapeake Bay region indicate a strong positive association between occurrence of proliferative liver lesions in this species and sediment polycyclic aromatic hydrocarbon (PAH) contamination. Highest prevalences of altered hepatocellular foci (AHF), adenomas and hepatocellular carcinomas/hepatoblastomas (HN) occurred in localized habitats most heavily contaminated with PAH of creosote origin. Additionally, biliary, exocrine pancreatic and vascular neoplasm prevalences were elevated in some PAH-contaminated habitats. Our recent long-term (1 year) laboratory exposures of mummichog to creosote-contaminated sediment and specific PAH-amended sediment and diet have provided some of the first direct experimental evidence for a cause and effect relationship between PAH exposoure and development of hepatic proliferative lesions including cancer in a wild fish species. Following 3 mo of continuous exposure to contaminated sediment and diet, mummichog exhibited no hepatic proliferative lesions. However, by 9 mo post-exposure, prevalence of AHF was elevated in both creosote-contaminated sediment (23%) and PAH-amended sediment/dietary (12%) exposures. At 12 months post-exposure AHF were further elevated in both treatments (40% and 30%, respectively) and hepatic neoplasms were first observed (7% and 2%, respectively). Based on our field and laboratory investigations, the Virginia Dept